- Email: [email protected]
Effect of Adrenocortical Steroids on Cystic and Papular Acne
EFFECT OF ADRENOCORTICAL STEROIDS ON CYSTIC AND PAPULAR ACNE JTILITJS L. DANTO, MD.
There is considerable evidence that androgenic hormones are of prime importance in acne. (1) Children who are castrated before puberty do not develop acne. However, if testosterone is administered to the eunuch he may develop acne. The administration of testosterone may also produce acne in normal males and females.
Some patients, while undergoing ACTH or corticosteroid therapy, have developed acneform lesions. (2, 3) However, Rothman noted that these eruptions differed from adolescent acne in that sehorrhea and comedones were not present; (4) and histologic examination of these lesions showed excessive follicular keratin-
ization and little if any sebaceous gland hyperfunction. (5) Numerous studies have been made on the effect of various hormones on the sebaceous glands of laboratory animals. Haskin, Lasker and Rothman found that in mature spayed female rats of a specific strain the subcutaneous injections of testosterone propionate produced an increase in the size of the sebaceous gland. Progesterone produced a similar increase in size. Cortisone caused a slight atrophy and ACTH produced a slight increase in the size of the gland. (5). Subsequently Rothman's group studied the effect of the pituitary-adrenal axis on the sebaceous glands in
white rats. (6) It was found that the sebaceous glands atrophied when the pituitary was removed in ovariectomized white rats. These atrophied glands could not be stimulated by progesterone and only slightly by testosterone. The administration of ACTH did not counteract these effects of pituitectomy on sehaceous glands. (7). The work done by Rothman and his associates suggests that the pituitary gland secretes a sebaceous gland trophic factor, which is important in making the sebaceous gland susceptible to stimulation by such hormones as testosterone and progesterone. Both cortisone and hydrocortisone have the ability to inhibit the output of pituitary adrenocorticotropin (8). The adrenocortical steroids are also capable of suppressing inflammation and depressing granulation tissue in the skin (8, 10). It is therefore conceivable that adequate dosages of cortisone or hydrocortisone might possibly make the sebaceous glands less susceptible to stimulation by androgenic hormones by inhibiting the secretions of the pituitary gland, and also suppress the inflammatory component of cystic and papular acne. METHOD
To test this hypothesis both cortisone and hydrocortisone* were administered to thirty-nine (39) patients with cystic aiid papular acne. This study included adolescent acne vulgaris and the "chin-type" of acne found in the older age group. Some of these patients had previously received standard acne treatment Received for publication March 1, 1957. * I wish to thank Pfizer & Co. for supplying the Hydrocortisone (Cortril) 315
316
THE JOURNAL OF INVESTIGATIVE DERMATOLOGY
CHART I Name
Steroid 'Daily DosageDaily Dosage Daily Dosage Daily Dosage Daily Dosage Daily dosage Used 1st week 2nd week 3rd week 4th week 5th week 6th week (mgs.)
1. J.L. 2. M.H.
6. A.S. 7. L.L.
E E E E E E E
8. D.B.
F
9.S.S.
E E E E E
3. Y.V. 4. MM.
5.J.L.
10. E.G. 11. P.C. 12. A.McL.
13. S.R. 14. B.S.
F
100
100 100 100 75 100 100 60 75 75
F
60
F
60
F
60 60 60 60 60 60 60 60 60 60 60 40
38. A.5.
F F F F F F F F F F F F F F F F F F E E
39. R.N.
E
20. J.T.
21. L.C. 22. E.P. 23. P.E. 24. R.5. 25. T.L.
26. M.L.
27. M.M. 28. R.D. 29. M.G. 30. J.K.
31. M.J.
32. M.B. 33. G.V. 34. J.W.
35. D.H. 36. L.G.
37. M.M.
(mgs.)
25
25
75(4 days) 50 (4 days) 25 (4 days) 75 50 25 75 50
75
25
25
60 50
50
F
J.K. 19. W.C.
(mgs.)
50
75 75
16. H.S.
18.
(rngs.)
75
50 50
15. P.s. C.L.F.
(mgs.)
75
75 60 60
17.
(mgs.)
60
40
40 60 60
60 40
60
60
40 40
60
40
20
60
60
40
60 60 60
60 40
60
60 40
60
40
75 75 75
* E: Cortisone
F: Hydrocortisone
others had received no previous treatment. Chart 1 records the dosage and scheoule for each patient. and
RESULTS
Of the fourteen patients who received cortisone, seven had an excellent response, six good, one fair. In the twenty-four cases receiving hydrocortisone, eleven had an excellent response, eight good, four fair, and one poor. (Chart 2)
CHART 2 Name
Sex
Age
Total
Type of Acne
Amount' Steroid
Duration Treatment
Result
Side Effect
(mgs.)
1. J.L. 2. M.H.
F 25 Cystic F 21 Cystic
E E
excellent none 1,300 three weeks excellent developed
2,430 six weeks
acneform
papules
3. Y.V. 4. M.M.
F 24 Cystic F 22 Cystic
E E
1,815 five weeks
excellent none
1,325 three and a half
fair
5. J.L.
E E E
1,055 two weeks 700 one week 700 one week
excellent none
6. A.S. 7. L.L.
F 24 Cystic F 45 Cystic F 24 Cystic
8. D.B.
F 21 Cystic and
F
840 two weeks
excellent none
E
675 two weeks
excellent none
9. S.S.
papular
F 20 Cystic and papular
none
weeks
good
fair
none developed papules
10. E.G.
F 38 Cystic
E
875 two weeks
good
11. P.C.
F 22 Papular
E E E
825 two weeks 525 one week 875 two weeks 420 one week 420 one week 420 one week
excellent none
700 two weeks 420 one week
excellent none
12. A.McL. F
Cystic
13. S.R. 14. B.S. 15. P.S. 16. H.S.
F 17 Cystic F 18 Papular
19. W.C.
M 19 Cystic and
20. J.T.
M 42 Cystic
M 19 Papular
F 30 Papular 17. C.L.F. F 33 Cystic F 22 Cystic 18. J.K. 21. L.C. 22. E.P.
papular
F 13 Papular
M 18 Papular
F F F F F F F F
F
and cystic
23. P.E.
F 13 Papular and F
24. ItS.
M 16 Cystic M 14 Cystic
F F
F 12 Papular
F F F F F
25. T.L. 26. M.L. 27. M.M.
28. R.l).
cystic
F
18 Cystic
F 15 Papular F 19 Cystic F 19 Papular F 16 Cystic
good good poor good
developed aeneform papules none none none none none none
fair 1,140 three weeks good 420 one week excellent none 420 one week fair none good
1,260 three weeks good
none developed some
pustules
1,120 three weeks excellent none
420 one week excellent none 1,260 three weeks good developed pustules none 420 one week good 700 two weeks 700 two weeks 280 one week
good good
none none none
F
fair 770 three weeks excellent none 1,120 three weeks excellent none 420 one week excellent none none 840 two weeks fair 700 two weeks excellent none
36. L.G.
F F
1,120 three weeks excellent none 700 two weeks excellent none
38. AS.
F 26 Cystic and E
39. R.N.
F 25 Papular
29. M.G.
30. J.K. 31. M.J. 32. J.B.
M 30 Cystic
F
33. G.V. 34. J.W.
F F 47 Cystic F 25 Papular and F
35. DII.
M 19
cystic Cystic
F 37 Cystic 37. MM. F 53 Cystic
papular
E E
525 one week 525 one week
good
none
excellent none
525 one week
good
none
Excellent: 75%—100% improvement; Good: 50%—75% improvement; Fair: 25%—50% improvement; Poor: 0%—25% improvement. 317
318
THE JOURNAL OF INVESPIGAPIVE DERMATOLOGY DISCUSSION AND CONCLUSION
The systemic administration of cortisone and hydrocortisone, caused regres-
sion of cystic and erythematous papular acne lesions. During the course of therapy five patients developed a small number of pustules in the acne areas. No signs of hypercorticalism were seen. In most cases there was a recurrence in variable degrees of cystic and papular lesions two to six weeks after the drugs were stopped. The lesions regressed with the readministration of the medication. This temporary remission of acne lesions with these adrenocortical steroids suggests that the mechanisms of action is through the anti-inflammatory effect of the drugs, and/or by the temporary suppression of the secretions of the pituitary gland thereby making the sebaceous glands less susceptible to stimulation by androgenic hormones. SUMMARY
Cortisone and hydrocortisone, were administered to thirty-nine (39) patients with acne lesions. These medications caused a temporary regression of cystic and erythematous papular lesions. Five cases developed pustules in the acne areas during therapy. The response of acne lesions to these adrenocortical steroids is believed to be due to their anti-inflammatory property and/or to the temporary suppression of the secretion of the pituitary gland. REFERENCES 1. HAMILTON, J.: Male hormone substance; A prime factor in acne. J. Clin. Endocrinol., 1:570—592, 1941.
2. BEUNNEE, M., RIDDELL, J., AND BEST, W.: Cutaneous side effects of ACTH, cortisone and progesterone therapy. J. Invest Dermat., 16: 205—210, 1951. 3. BEHEMAN, H. I., AND GOODMAN, J. J.: Skin complications of cortisone and ACTH therapy. J.A.M.A., 144: 218—221, 1950. 4. ROTHMAN, S. Discussion of paper by Brunsting, H. A. Hidradenitis and uther variants
of acne. Arch. Dermat. & Syph., 65: 303, 1952. 5. H.scia', D., LASMEE, N., AND ROTMMAN, S.: Some effects of ACTH, cortisone, proges-
terone and testosterone on sebaceous glands in the white rat. J. Invest. Dermat., 20: 207—211, 1953.
6. LAsHER, N., LoRINcz, A. L. AND ROTHMAN, S.: Hormonal effects of sebaceous glands in
the white rat. The effect of the pituitary-adrenal axis. J. Invest. Dermat., 22: 25—29, 1954.
7. LA5MEE, N., LoalNcz, A. L. AND ROTHMAN, S.: Hormonal effects on sebaceous glands in
the white rat. Evidence for the presence of a pituitary sebaceous gland trophic factor. J. Invest. Dermat., 24: 499—505, 1955.
8. SPRAGUE, R. G., et al: Observations on the physiologic effects of cortisone and ACTH in man. Arch. Tnt. Med., 85: 199—258, 1950.
9. CAUvALLERO, C.: The Mechanisms of Inflammation, pg. 259. ACTA Inc., Medical Publishers Montreal. 10. SELYE, H.: The part of Inflammation in the Local Adaptation Syndrome, pg. 53—74. The Mechanism of Inflammation. ACTA, Inc., Medical Publishers Montreal.
THE JOURNAL OF INVESTIGATIVE DERMATOLOGY
94
linolenic acid extract. Arch. This pdf is a scanned copy UV of irradiated a printed document.
24. Wynn, C. H. and Iqbal, M.: Isolation of rat
skin lysosomes and a comparison with liver Path., 80: 91, 1965. and spleen lysosomes. Biochem. J., 98: lOP, 37. Nicolaides, N.: Lipids, membranes, and the 1966.
human epidermis, p. 511, The Epidermis
Eds., Montagna, W. and Lobitz, W. C. Acascopic localization of acid phosphatase in demic Press, New York. human epidermis. J. Invest. Derm., 46: 431, 38. Wills, E. D. and Wilkinson, A. E.: Release of 1966. enzymes from lysosomes by irradiation and 26. Rowden, C.: Ultrastructural studies of kerathe relation of lipid peroxide formation to tinized epithelia of the mouse. I. Combined enzyme release. Biochem. J., 99: 657, 1966. electron microscope and cytochemical study 39. Lane, N. I. and Novikoff, A. B.: Effects of of lysosomes in mouse epidermis and esoarginine deprivation, ultraviolet radiation and X-radiation on cultured KB cells. J. phageal epithelium. J. Invest. Derm., 49: 181, 25. Olson, R. L. and Nordquist, R. E.: Ultramicro-
No warranty is given about the accuracy of the copy.
Users should refer to the original published dermal cells. Nature, 216: 1031, 1967. version of1965. the material. vest. Derm., 45: 448, 28. Hall, J. H., Smith, J. G., Jr. and Burnett, S. 41. Daniels, F., Jr. and Johnson, B. E.: In prepa1967.
Cell Biol., 27: 603, 1965.
27. Prose, P. H., Sedlis, E. and Bigelow, M.: The 40. Fukuyama, K., Epstein, W. L. and Epstein, demonstration of lysosomes in the diseased J. H.: Effect of ultraviolet light on RNA skin of infants with infantile eczema. J. Inand protein synthesis in differentiated epi-
C.: The lysosome in contact dermatitis: A ration. histochemical study. J. Invest. Derm., 49: 42. Ito, M.: Histochemical investigations of Unna's oxygen and reduction areas by means of 590, 1967. 29. Pearse, A. C. E.: p. 882, Histochemistry Theoultraviolet irradiation, Studies on Melanin, retical and Applied, 2nd ed., Churchill, London, 1960.
30. Pearse, A. C. E.: p. 910, Histacheini.stry Thearetscal and Applied, 2nd ed., Churchill, London, 1960.
31. Daniels, F., Jr., Brophy, D. and Lobitz, W. C.: Histochemical responses of human skin fol-
lowing ultraviolet irradiation. J. Invest. Derm.,37: 351, 1961.
32. Bitensky, L.: The demonstration of lysosomes by the controlled temperature freezing section method. Quart. J. Micr. Sci., 103: 205, 1952.
33. Diengdoh, J. V.: The demonstration of lysosomes in mouse skin. Quart. J. Micr. Sci., 105: 73, 1964.
34. Jarret, A., Spearman, R. I. C. and Hardy, J. A.:
Tohoku, J. Exp. Med., 65: Supplement V, 10, 1957.
43. Bitcnsky, L.: Lysosomes in normal and pathological cells, pp. 362—375, Lysasames Eds., de Reuck, A. V. S. and Cameron, M. Churchill, London, 1953.
44. Janoff, A. and Zweifach, B. W.: Production of inflammatory changes in the microcirculation by cationic proteins extracted from lysosomes. J. Exp. Med., 120: 747, 1964.
45. Herion, J. C., Spitznagel, J. K., Walker, R. I. and Zeya, H. I.: Pyrogenicity of granulocyte lysosomes. Amer. J. Physiol., 211: 693, 1966.
46. Baden, H. P. and Pearlman, C.: The effect of ultraviolet light on protein and nucleic acid synthesis in the epidermis. J. Invest. Derm.,
Histochemistry of keratinization. Brit. J. 43: 71, 1964. Derm., 71: 277, 1959. 35. De Duve, C. and Wattiaux, R.: Functions of 47. Bullough, W. S. and Laurence, E. B.: Mitotic control by internal secretion: the role of lysosomes. Ann. Rev. Physiol., 28: 435, 1966. the chalone-adrenalin complex. Exp. Cell. 36. Waravdekar, V. S., Saclaw, L. D., Jones, W. A. and Kuhns, J. C.: Skin changes induced by
Res., 33: 176, 1964.
There is considerable evidence that androgenic hormones are of prime importance in acne. (1) Children who are castrated before puberty do not develop acne. However, if testosterone is administered to the eunuch he may develop acne. The administration of testosterone may also produce acne in normal males and females.
Some patients, while undergoing ACTH or corticosteroid therapy, have developed acneform lesions. (2, 3) However, Rothman noted that these eruptions differed from adolescent acne in that sehorrhea and comedones were not present; (4) and histologic examination of these lesions showed excessive follicular keratin-
ization and little if any sebaceous gland hyperfunction. (5) Numerous studies have been made on the effect of various hormones on the sebaceous glands of laboratory animals. Haskin, Lasker and Rothman found that in mature spayed female rats of a specific strain the subcutaneous injections of testosterone propionate produced an increase in the size of the sebaceous gland. Progesterone produced a similar increase in size. Cortisone caused a slight atrophy and ACTH produced a slight increase in the size of the gland. (5). Subsequently Rothman's group studied the effect of the pituitary-adrenal axis on the sebaceous glands in
white rats. (6) It was found that the sebaceous glands atrophied when the pituitary was removed in ovariectomized white rats. These atrophied glands could not be stimulated by progesterone and only slightly by testosterone. The administration of ACTH did not counteract these effects of pituitectomy on sehaceous glands. (7). The work done by Rothman and his associates suggests that the pituitary gland secretes a sebaceous gland trophic factor, which is important in making the sebaceous gland susceptible to stimulation by such hormones as testosterone and progesterone. Both cortisone and hydrocortisone have the ability to inhibit the output of pituitary adrenocorticotropin (8). The adrenocortical steroids are also capable of suppressing inflammation and depressing granulation tissue in the skin (8, 10). It is therefore conceivable that adequate dosages of cortisone or hydrocortisone might possibly make the sebaceous glands less susceptible to stimulation by androgenic hormones by inhibiting the secretions of the pituitary gland, and also suppress the inflammatory component of cystic and papular acne. METHOD
To test this hypothesis both cortisone and hydrocortisone* were administered to thirty-nine (39) patients with cystic aiid papular acne. This study included adolescent acne vulgaris and the "chin-type" of acne found in the older age group. Some of these patients had previously received standard acne treatment Received for publication March 1, 1957. * I wish to thank Pfizer & Co. for supplying the Hydrocortisone (Cortril) 315
316
THE JOURNAL OF INVESTIGATIVE DERMATOLOGY
CHART I Name
Steroid 'Daily DosageDaily Dosage Daily Dosage Daily Dosage Daily Dosage Daily dosage Used 1st week 2nd week 3rd week 4th week 5th week 6th week (mgs.)
1. J.L. 2. M.H.
6. A.S. 7. L.L.
E E E E E E E
8. D.B.
F
9.S.S.
E E E E E
3. Y.V. 4. MM.
5.J.L.
10. E.G. 11. P.C. 12. A.McL.
13. S.R. 14. B.S.
F
100
100 100 100 75 100 100 60 75 75
F
60
F
60
F
60 60 60 60 60 60 60 60 60 60 60 40
38. A.5.
F F F F F F F F F F F F F F F F F F E E
39. R.N.
E
20. J.T.
21. L.C. 22. E.P. 23. P.E. 24. R.5. 25. T.L.
26. M.L.
27. M.M. 28. R.D. 29. M.G. 30. J.K.
31. M.J.
32. M.B. 33. G.V. 34. J.W.
35. D.H. 36. L.G.
37. M.M.
(mgs.)
25
25
75(4 days) 50 (4 days) 25 (4 days) 75 50 25 75 50
75
25
25
60 50
50
F
J.K. 19. W.C.
(mgs.)
50
75 75
16. H.S.
18.
(rngs.)
75
50 50
15. P.s. C.L.F.
(mgs.)
75
75 60 60
17.
(mgs.)
60
40
40 60 60
60 40
60
60
40 40
60
40
20
60
60
40
60 60 60
60 40
60
60 40
60
40
75 75 75
* E: Cortisone
F: Hydrocortisone
others had received no previous treatment. Chart 1 records the dosage and scheoule for each patient. and
RESULTS
Of the fourteen patients who received cortisone, seven had an excellent response, six good, one fair. In the twenty-four cases receiving hydrocortisone, eleven had an excellent response, eight good, four fair, and one poor. (Chart 2)
CHART 2 Name
Sex
Age
Total
Type of Acne
Amount' Steroid
Duration Treatment
Result
Side Effect
(mgs.)
1. J.L. 2. M.H.
F 25 Cystic F 21 Cystic
E E
excellent none 1,300 three weeks excellent developed
2,430 six weeks
acneform
papules
3. Y.V. 4. M.M.
F 24 Cystic F 22 Cystic
E E
1,815 five weeks
excellent none
1,325 three and a half
fair
5. J.L.
E E E
1,055 two weeks 700 one week 700 one week
excellent none
6. A.S. 7. L.L.
F 24 Cystic F 45 Cystic F 24 Cystic
8. D.B.
F 21 Cystic and
F
840 two weeks
excellent none
E
675 two weeks
excellent none
9. S.S.
papular
F 20 Cystic and papular
none
weeks
good
fair
none developed papules
10. E.G.
F 38 Cystic
E
875 two weeks
good
11. P.C.
F 22 Papular
E E E
825 two weeks 525 one week 875 two weeks 420 one week 420 one week 420 one week
excellent none
700 two weeks 420 one week
excellent none
12. A.McL. F
Cystic
13. S.R. 14. B.S. 15. P.S. 16. H.S.
F 17 Cystic F 18 Papular
19. W.C.
M 19 Cystic and
20. J.T.
M 42 Cystic
M 19 Papular
F 30 Papular 17. C.L.F. F 33 Cystic F 22 Cystic 18. J.K. 21. L.C. 22. E.P.
papular
F 13 Papular
M 18 Papular
F F F F F F F F
F
and cystic
23. P.E.
F 13 Papular and F
24. ItS.
M 16 Cystic M 14 Cystic
F F
F 12 Papular
F F F F F
25. T.L. 26. M.L. 27. M.M.
28. R.l).
cystic
F
18 Cystic
F 15 Papular F 19 Cystic F 19 Papular F 16 Cystic
good good poor good
developed aeneform papules none none none none none none
fair 1,140 three weeks good 420 one week excellent none 420 one week fair none good
1,260 three weeks good
none developed some
pustules
1,120 three weeks excellent none
420 one week excellent none 1,260 three weeks good developed pustules none 420 one week good 700 two weeks 700 two weeks 280 one week
good good
none none none
F
fair 770 three weeks excellent none 1,120 three weeks excellent none 420 one week excellent none none 840 two weeks fair 700 two weeks excellent none
36. L.G.
F F
1,120 three weeks excellent none 700 two weeks excellent none
38. AS.
F 26 Cystic and E
39. R.N.
F 25 Papular
29. M.G.
30. J.K. 31. M.J. 32. J.B.
M 30 Cystic
F
33. G.V. 34. J.W.
F F 47 Cystic F 25 Papular and F
35. DII.
M 19
cystic Cystic
F 37 Cystic 37. MM. F 53 Cystic
papular
E E
525 one week 525 one week
good
none
excellent none
525 one week
good
none
Excellent: 75%—100% improvement; Good: 50%—75% improvement; Fair: 25%—50% improvement; Poor: 0%—25% improvement. 317
318
THE JOURNAL OF INVESPIGAPIVE DERMATOLOGY DISCUSSION AND CONCLUSION
The systemic administration of cortisone and hydrocortisone, caused regres-
sion of cystic and erythematous papular acne lesions. During the course of therapy five patients developed a small number of pustules in the acne areas. No signs of hypercorticalism were seen. In most cases there was a recurrence in variable degrees of cystic and papular lesions two to six weeks after the drugs were stopped. The lesions regressed with the readministration of the medication. This temporary remission of acne lesions with these adrenocortical steroids suggests that the mechanisms of action is through the anti-inflammatory effect of the drugs, and/or by the temporary suppression of the secretions of the pituitary gland thereby making the sebaceous glands less susceptible to stimulation by androgenic hormones. SUMMARY
Cortisone and hydrocortisone, were administered to thirty-nine (39) patients with acne lesions. These medications caused a temporary regression of cystic and erythematous papular lesions. Five cases developed pustules in the acne areas during therapy. The response of acne lesions to these adrenocortical steroids is believed to be due to their anti-inflammatory property and/or to the temporary suppression of the secretion of the pituitary gland. REFERENCES 1. HAMILTON, J.: Male hormone substance; A prime factor in acne. J. Clin. Endocrinol., 1:570—592, 1941.
2. BEUNNEE, M., RIDDELL, J., AND BEST, W.: Cutaneous side effects of ACTH, cortisone and progesterone therapy. J. Invest Dermat., 16: 205—210, 1951. 3. BEHEMAN, H. I., AND GOODMAN, J. J.: Skin complications of cortisone and ACTH therapy. J.A.M.A., 144: 218—221, 1950. 4. ROTHMAN, S. Discussion of paper by Brunsting, H. A. Hidradenitis and uther variants
of acne. Arch. Dermat. & Syph., 65: 303, 1952. 5. H.scia', D., LASMEE, N., AND ROTMMAN, S.: Some effects of ACTH, cortisone, proges-
terone and testosterone on sebaceous glands in the white rat. J. Invest. Dermat., 20: 207—211, 1953.
6. LAsHER, N., LoRINcz, A. L. AND ROTHMAN, S.: Hormonal effects of sebaceous glands in
the white rat. The effect of the pituitary-adrenal axis. J. Invest. Dermat., 22: 25—29, 1954.
7. LA5MEE, N., LoalNcz, A. L. AND ROTHMAN, S.: Hormonal effects on sebaceous glands in
the white rat. Evidence for the presence of a pituitary sebaceous gland trophic factor. J. Invest. Dermat., 24: 499—505, 1955.
8. SPRAGUE, R. G., et al: Observations on the physiologic effects of cortisone and ACTH in man. Arch. Tnt. Med., 85: 199—258, 1950.
9. CAUvALLERO, C.: The Mechanisms of Inflammation, pg. 259. ACTA Inc., Medical Publishers Montreal. 10. SELYE, H.: The part of Inflammation in the Local Adaptation Syndrome, pg. 53—74. The Mechanism of Inflammation. ACTA, Inc., Medical Publishers Montreal.
THE JOURNAL OF INVESTIGATIVE DERMATOLOGY
94
linolenic acid extract. Arch. This pdf is a scanned copy UV of irradiated a printed document.
24. Wynn, C. H. and Iqbal, M.: Isolation of rat
skin lysosomes and a comparison with liver Path., 80: 91, 1965. and spleen lysosomes. Biochem. J., 98: lOP, 37. Nicolaides, N.: Lipids, membranes, and the 1966.
human epidermis, p. 511, The Epidermis
Eds., Montagna, W. and Lobitz, W. C. Acascopic localization of acid phosphatase in demic Press, New York. human epidermis. J. Invest. Derm., 46: 431, 38. Wills, E. D. and Wilkinson, A. E.: Release of 1966. enzymes from lysosomes by irradiation and 26. Rowden, C.: Ultrastructural studies of kerathe relation of lipid peroxide formation to tinized epithelia of the mouse. I. Combined enzyme release. Biochem. J., 99: 657, 1966. electron microscope and cytochemical study 39. Lane, N. I. and Novikoff, A. B.: Effects of of lysosomes in mouse epidermis and esoarginine deprivation, ultraviolet radiation and X-radiation on cultured KB cells. J. phageal epithelium. J. Invest. Derm., 49: 181, 25. Olson, R. L. and Nordquist, R. E.: Ultramicro-
No warranty is given about the accuracy of the copy.
Users should refer to the original published dermal cells. Nature, 216: 1031, 1967. version of1965. the material. vest. Derm., 45: 448, 28. Hall, J. H., Smith, J. G., Jr. and Burnett, S. 41. Daniels, F., Jr. and Johnson, B. E.: In prepa1967.
Cell Biol., 27: 603, 1965.
27. Prose, P. H., Sedlis, E. and Bigelow, M.: The 40. Fukuyama, K., Epstein, W. L. and Epstein, demonstration of lysosomes in the diseased J. H.: Effect of ultraviolet light on RNA skin of infants with infantile eczema. J. Inand protein synthesis in differentiated epi-
C.: The lysosome in contact dermatitis: A ration. histochemical study. J. Invest. Derm., 49: 42. Ito, M.: Histochemical investigations of Unna's oxygen and reduction areas by means of 590, 1967. 29. Pearse, A. C. E.: p. 882, Histochemistry Theoultraviolet irradiation, Studies on Melanin, retical and Applied, 2nd ed., Churchill, London, 1960.
30. Pearse, A. C. E.: p. 910, Histacheini.stry Thearetscal and Applied, 2nd ed., Churchill, London, 1960.
31. Daniels, F., Jr., Brophy, D. and Lobitz, W. C.: Histochemical responses of human skin fol-
lowing ultraviolet irradiation. J. Invest. Derm.,37: 351, 1961.
32. Bitensky, L.: The demonstration of lysosomes by the controlled temperature freezing section method. Quart. J. Micr. Sci., 103: 205, 1952.
33. Diengdoh, J. V.: The demonstration of lysosomes in mouse skin. Quart. J. Micr. Sci., 105: 73, 1964.
34. Jarret, A., Spearman, R. I. C. and Hardy, J. A.:
Tohoku, J. Exp. Med., 65: Supplement V, 10, 1957.
43. Bitcnsky, L.: Lysosomes in normal and pathological cells, pp. 362—375, Lysasames Eds., de Reuck, A. V. S. and Cameron, M. Churchill, London, 1953.
44. Janoff, A. and Zweifach, B. W.: Production of inflammatory changes in the microcirculation by cationic proteins extracted from lysosomes. J. Exp. Med., 120: 747, 1964.
45. Herion, J. C., Spitznagel, J. K., Walker, R. I. and Zeya, H. I.: Pyrogenicity of granulocyte lysosomes. Amer. J. Physiol., 211: 693, 1966.
46. Baden, H. P. and Pearlman, C.: The effect of ultraviolet light on protein and nucleic acid synthesis in the epidermis. J. Invest. Derm.,
Histochemistry of keratinization. Brit. J. 43: 71, 1964. Derm., 71: 277, 1959. 35. De Duve, C. and Wattiaux, R.: Functions of 47. Bullough, W. S. and Laurence, E. B.: Mitotic control by internal secretion: the role of lysosomes. Ann. Rev. Physiol., 28: 435, 1966. the chalone-adrenalin complex. Exp. Cell. 36. Waravdekar, V. S., Saclaw, L. D., Jones, W. A. and Kuhns, J. C.: Skin changes induced by
Res., 33: 176, 1964.